The Role of HDAC3-Akt Signaling Pathway in Proliferation of Vascular Smooth Muscle Cells
10.3870/j.issn.1672-0741.24.07.020
- VernacularTitle:HDAC3-Akt通路在血管平滑肌细胞增殖中的作用
- Author:
Fengjiao TAN
1
;
Bo HUO
;
Dingsheng JIANG
Author Information
1. 武汉科技大学附属天佑医院心胸外科,武汉 430081
- Publication Type:Journal Article
- Keywords:
vascular smooth muscle cell;
cell proliferation;
HDAC3;
Akt
- From:
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
2025;54(4):465-469
- CountryChina
- Language:Chinese
-
Abstract:
Objective To examine the mechanism by which the HDAC3-Akt signaling pathway regulates the proliferation of aortic smooth muscle cells.Methods Rabbit vascular smooth muscle cells(rVSMCs)were subjected to various treatments,in-cluding DMSO(control),RGFP966(HDAC3 inhibitor),Flag(control for gene intervention),HDAC3 overexpression,and HDAC3 overexpression combined with Akt inhibitor MK2206.The5-Ethynyl-2'-deoxyuridine(EdU)assay and thecell counting assay were used to detect the proliferative capacity of cells in each group.The expression level of PCNA,p-H3,Akt and p-Akt in each group were examined by Western blotting.Results Compared with the control group(DMSO),the expression levels of p-Akt,PCNA,and p-H3 in the RGFP966 inhibitor group were significantly decreased(all P＜0.05).Concurrently,both the cell counting and EdU assays demonstrated a reduction in proliferation in the RGFP966-treated group compared to the DMSO group(both P＜0.05).In contrast,the HDAC3 overexpression group exhibited a significant increase in the expression levels of p-Akt,PCNA,and p-H3 compared to the Flag group(all P＜0.05).Cell counting assay and EdU assay showed that the prolifera-tion level in the HDAC3 overexpression group was elevated compared with the Flag group(both P＜0.05).Akt inhibitor MK2206 could reversed this effect induced by HDAC3 overexpression.Conclusion HDAC3 can effectively promote the prolif-eration of aortic smooth muscle cells,which might be mediated through Akt signaling pathway.
